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Metabolic Interrelationships of Starve-Feed Cycle
- 2. Not all of the major metabolic pathways operate in every tissue at any given time. The metabolic processes i.e; glycogenesis, glycogenolysis, gluconeogenesis, glycolysis, fatty acid synthesis, lipogenesis, lipolysis, fatty acid oxidation, TCA cycle activity, ketogenesis, amino acid oxidation, protein synthesis, and urea synthesis. It is important to know (1) which tissues are most active in these various processes, (2) when these processes are most or least active, and (3) how these processes are controlled and coordinated in different metabolic states. Hence, the metabolism of the starve-feed cycle Overview
- 3. the starve–feed cycle allows a variable fuel and nitrogen consumption to meet a variable metabolic and anabolic demand. Also there is, ATP cycle within the starve–feed cycle; which provides the energy for utilization.
- 4. In the well-fed state the Diet supplies the energy requirement. the fate of glucose, amino acids, and fat obtained from food. 1) Glucose passes from the intestinal epithelial cells to the liver by way of the portal vein. 2) Amino acids are partially metabolized in the gut before being released into portal blood. 3) Chylomicrons, that contain TAG is secreted by the intestinal epithelial cells into lymphatics thoracic duct subclavian vein rest of the body. Starve-Feed Cycle
- 5. In the liver, Glucose forms: 1) Glycogen by glycogenesis 2) Pyruvate and lactate by glycolysis 3) Pentose phosphate pathway 4) Pyruvate is oxidized to acetyl CoA which can form TAG or oxidized to CO2 and H20 by TCA cycle. In the well-fed state, the liver uses glucose and does not engage in gluconeogenesis. Thus, Cori cycle (glucose to lactate and vice versa) is interrupted in this state.
- 6. From intestinal cells, Amino acids, 1) Move to the portal vein 2) Some amino acids are taken up by the liver while others pass through. (EAAs needed for protein synthesis) 3) Liver metabolizes amino acids but for that they have to be present in high conc. Before catabolism can occur. 4) Protein synthesis can occur as long as all the amino acids are present. 5) If excess, then oxidation occurs to Co2, H2O, urea.
- 7. Chylomicrons contain TAG, which in turn are acted upon by Lipoprotein lipase (Lpl) which are found in the endothelial cells of capillaries. 1) Large portions of TAG are hydrolyzed but not all present in the chylomicrons. 2) Released fatty acids are taken up by adipocytes, reesterified to Glycerol 3- phosphate to TAG, and stored as fat droplets. 3) The chylomicron remnant in the blood is cleared by the liver. 4) Then TAG are packaged into VLDL, and released into the blood. 5) In adipocytes, Lpl can act on VLDL and store fat droplets.
- 8. β cells of pancreas 1) When glucose enters the beta cell, its oxidation raise the ATP level, closes the ATP-sensitive potassium channel, depolarizes the cell and causes influx of calcium, leading to insulin release. 2) Insulin is released during and after eating.
- 9. Hepatic glycogenolysis maintains blood glucose during early fasting. Lactate, pyruvate, alanine are diverted from oxidation and fatty acid synthesis into glucose formation. Alanine cycle in which carbon and nitrogen return to the liver. In The Early Fasting State
- 10. After10-12h of fasting, there is little glycogen left in the liver, the body is dependent on hepatic gluconeogenesis. Cori cycle and alanine cycle play and important role don’t provide carbons for glucose. F.As energy from the liver is transferred to the peripheral tissue. In the brain glucose from the brain is oxidized to CO2 and H2O. Glycerol released for adipose tissue, provides the carbons for glucose synthesis. In muscles tissues, proteins are hydrolyzed to amino acids, which release glutamine and alanine in large amounts. Metabolic Interrelationships of Major Tissues in Fasting State
- 11. Part of glutamine is taken up by the intestinal cells and used by enterocytes for the synthesis of purines and pyrimidines. Glutamine is converted to glutamate which is transaminated with pyruvate to form alpha- ketoglutarate and alanine. Alpha-ketoglutaratemalatepyruvate, in TCA cycle. Pyruvate is used by enterocytes to form alanine. This is called Glutaminolysis pathway, (partial oxidation) In Enterocytes Fig: Enterocytes
- 12. Glutaminolysis with aspartate is used by lymphocytes and macrophages to meet energy needs. Aspartate, is used in nucleotide synthesis. Glutamine is transaminated with alpha- ketoglutarate to form glutamate, releasing an amino group and a keto-acid for glucose synthesis. Glutamatealpha-ketoglutarate by glutamate dyhydrogenase. OAA is transaminated to aspartate by aspartate aminotransferase Glutamate provides 2N for urea synthesis, and precursor for ornithine such as citrulline. In Lymphocytes Fig: Lymphocytes
- 13. In the intestinal epithelium, glutamate + NADPH + H* + ATP glutamate semi- aldehyde + NAD* + ADP + Pi (ATP- dependent step). Citrulline is released from the gut. In the kidneys, citrulline arginine creatin which is released into the blood. The liver uses arginine to form ornithine which expands the urea cycle capacity. The liver can irreversibly covert, Ornithine(transamination)glutamate semi- aldehydeglutamate Inter-organ Metabolic Interactions
- 14. GSH is important in detoxification of chemical compounds. Liver is the major synthesizer of GSH from glutamate, cysteine, glycine. The liver uses dietary methionine to form cysteine via cystathionine pathway. Hepatic GSH is released into the blood stream and distributed to other tissues; it is also released with bile into the gut. Enterocytes take up GSH from the intestinal lumen. Glutathione (GSH)
- 15. Carnitine Is derived from residues of various proteins. The proteins are Methylated using S- adinosylmethionine (SAM) to form trimethyllysine (TML) residues. TML γ-Butyrobetaine aldehyde + glycine which forms carnithine Liver and kidneys complete the entire pathway. Skeletal muscles release γ-Butyrobetaine aldehyde so that the liver and kidneys can form carnitine.
- 16. The constant availability of fuel in the blood is termed as caloric homeostasis. An average person requires, Caloric Homeostasis Stored fuel Tissue (g) (Kcal) Glycogen Liver 70 280 Glycogen Muscle 120 480 Glucose Body fluids 20 80 Fat Adipose 15,000 135,000 Protein Muscle 6,000 24,000
- 17. Effects of starvation on glucose homeostasis has been divided into five stages: Glucose Homeostasis Phase Origin of Blood Glucose Tissue using Glucose Major fuel of Brain 1 Exogensis All Glucose 2 Glycogen Hepatic – guconeogensis All except liver, Muscles & adipose tissue at diminished rate Glucose 3 Hepatic gluconeogenesis Glycogen All except liver, Muscle & adipose tissue At intermediate rate Glucose 4 Gluconeogensis, Hepatic & Renal Brain, RBCs, Renal medulla, little by muscle Glucose, ketone bodies 5 Gluconeogensis, Hepatic & Renal Brain at diminished rate, RBCs, Renal medulla Ketone bodies glucose